ArticleNature chemical biology2018
Allosteric mechanisms underlie GPCR signaling to SH3-domain proteins through arrestin.
Article in Nature chemical biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- Arrestins as programmable integrators of GPCR signaling: structural microstates, spatiotemporal logic, and therapeutic control.Cell discovery · 2026Review
- Mechanism of beta-arrestin 1 mediated Src activation via Src SH3 domain revealed by cryo-electron microscopy.Nature communications · 2026Article
- GPCR Phospho-Barcodes and Biased Signaling.Handbook of experimental pharmacology · 2026Review
- Mechanism of beta-arrestin 1 mediated Src activation via Src SH3 domain revealed by cryo-electron microscopy.bioRxiv : the preprint server for biology · 2025Article
- G protein-coupled receptors: pivotal hubs in gastric cancer malignancy-from multidimensional crosstalk to precision therapeutics.Journal of translational medicine · 2025Review
- Genetic Code Expansion: Recent Developments and Emerging Applications.Chemical reviews · 2025Review
- β-arrestins Are Scaffolding Proteins Required for Shh-Mediated Axon Guidance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Beneath the surface: endosomal GPCR signaling.Trends in biochemical sciences · 2024Review
- Distinct activation mechanisms of β-arrestin-1 revealed byNature communications · 2023Article
- Signal transduction at GPCRs: Allosteric activation of the ERK MAPK by β-arrestin.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The role of G protein-coupled receptor in neutrophil dysfunction during sepsis-induced acute respiratory distress syndrome.Frontiers in immunology · 2023Review
- Exploring the diversity of AVPR2 in Primates and its evolutionary implications.Genetics and molecular biology · 2023Article
- Discrete GPCR-triggered endocytic modes enable β-arrestins to flexibly regulate cell signaling.eLife · 2022Article
- G-Protein Coupled Receptors in Human Sperm: An In Silico Approach to Identify Potential Modulatory Targets.Molecules (Basel, Switzerland) · 2022Article
- G protein-coupled receptor signaling: transducers and effectors.American journal of physiology. Cell physiology · 2022Review
- Serodolin, a β-arrestin-biased ligand of 5-HTProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Progesterone activates GPR126 to promote breast cancer development via the Gi pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- QR code model: a new possibility for GPCR phosphorylation recognition.Cell communication and signaling : CCS · 2022Review
- Activation of PTH1R alleviates epididymitis and orchitis through Gq and β-arrestin-1 pathways.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Scaffolding mechanism of arrestin-2 in the cRaf/MEK1/ERK signaling cascade.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signals from 800 G-protein-coupled receptors (GPCRs) to many SH3 domain-containing proteins (SH3-CPs) regulate important physiological functions. These GPCRs may share a common pathway by signaling to SH3-CPs via agonist-dependent arrestin recruitment rather than through direct interactions. In the present study,
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.